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21 publications mentioning mmu-mir-431

Open access articles that are associated with the species Mus musculus and mention the gene name mir-431. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 315
We detected 2.4-fold upregulation of miR-431, a twofold upregulation of miR-744, and a 2.5-fold upregulation of miR-21, respectively (Figure 1B). [score:10]
Additionally, blocking miR-431 activity with miR-431 inhibitor significantly inhibited neurite extension (no treatment control group: 100 ± 5%; miR-431 mimic group: 130 ± 6%; mimic negative group: 91 ± 4%; miR-431 inhibitor group: 75% ± 7%; inhibitor negative control: 90 ± 8%; Figure 2B). [score:9]
miR-431 MODULATES Kremen1 EXPRESSION AT mRNA AND PROTEIN LEVELS IN PRIMARY NEURONAL CULTURESTo show that miR-431 regulates endogenous Kremen1 in DRG neurons, we transfected cells with either miR-431 mimics, miR-431 inhibitors, mimic negative control, or inhibitor negative control. [score:8]
Analyses of 24 putative targets of miR-431, showed that only six were suppressed in PC12 cells and even less genes were suppressed in DRG primary neurons. [score:7]
Moreover, manipulating miRNA-431 levels also affected axon branching, and led to a decrease in the number of branches per neuron due to transfection with miR-431 inhibitor (no treatment control group: 100 ± 9%; miR-431 mimic group: 110 ± 10%; mimic negative group: 82 ± 7%; miR-431 inhibitor group: 64% ± 6%; inhibitor negative control: 86 ± 10%; Figure 2C). [score:7]
In the RT-qPCR experiments, overexpression of miR-431 led to significant suppression of the expression of only three genes including Braf, Kremen1, and Zkscan1 (Table 1). [score:7]
We hypothesized that an increased expression of miR-431 in pre-conditioned DRG, would negatively associate with expression of the target mRNAs in the same RNA samples. [score:7]
We next studied GAP-43 expression in DRG neurons with miR-431 mimic and inhibitor treatments, as a strong association between neurite outgrowth and expression of GAP-43 has been reported in previous studies (Benowitz and Routtenberg, 1997). [score:7]
Whereas endogenous miR-431 was inhibited by transfection with miR-431 inhibitor, the expression level of the Kremen1 protein was significantly higher than in control groups. [score:7]
Since miRNA -mediated gene regulation can destabilize target mRNA and reduce the level of the target mRNA, we used RT-qPCR to determine the effect of miR-431 on Kremen1. [score:6]
These 24 genes met both criteria, of having a predicted binding site for miR-431 in their 3′-UTR and significantly down-regulated expression level in DRG microarray (Figure 1C). [score:6]
To show that miR-431 regulates endogenous Kremen1 in DRG neurons, we transfected cells with either miR-431 mimics, miR-431 inhibitors, mimic negative control, or inhibitor negative control. [score:6]
miR-431 was upregulated by the addition of human fibroblast interferon (HuIFN-β) in a non-cancer HuIFN-β sensitive cell line RSa, with concomitant suppression of IGF1R signaling and reduction of cell viability (Tanaka et al., 2012). [score:6]
Kremen1 expression was down-regulated by miR-431 at the mRNA and protein levels. [score:6]
Overlap shows 24 genes having predicted binding site for miR-431 and significantly down-regulated expression level in DRG microarray. [score:6]
This could be related to the specificity of miR-431 to these genes, and to the fact that down-regulation of less specific targets is more easily detected in PC12 cells. [score:6]
Collectively, our observations provide the first evidence for a role of miRNA in regulating Wnt/beta-catenin signaling pathway in nerve regeneration and identify miR-431 as an important regulator and a potential therapeutic target. [score:5]
Cells transfected with miR-431 mimics had decreased protein level of Kremen1, whiles cells transfected with miR-431 inhibitors had an increased expression of Kremen1. [score:5]
Overexpression of miR-431 significantly increased axon extension, whereas suppression of miR-431 significantly blocked axon branching. [score:5]
On the contrary, suppression of miR-431 activity significantly enhanced the expression of Kremen1 mRNA. [score:5]
On the other hand, inhibition of endogenous miR-431 resulted in a significant increase of Kremen1 expression by 45% (Figures 3D, E). [score:5]
The most upregulated miR-431 was selected for further analyses. [score:4]
To investigate which genes may be regulated by miR-431, we initially screened potential targets in neuronal PC12 cells overexpressing miR-431. [score:4]
Treatment of miR-431 mimics in DRG neuronal cultures significantly inhibited Kremen1 expression as compared with that of control groups. [score:4]
In agreement with the microarray data, miR-431, miR-744, and miR-21 were significantly upregulated in regenerating neuronal cells. [score:4]
Both miR-21 and miR-431 showed significant upregulation in DRG after SNI, comparably to our current data. [score:4]
Recent observation has linked expression of miR-431 to regulation of cell viability (Tanaka et al., 2012). [score:4]
To the best of our knowledge this is the first observation of direct mRNA target cleavage by miR-431. [score:4]
Taken together, our studies identified miR-431 as an endogenous, injury-regulated inhibitor of Kremen1, which promotes regenerative axon growth in adult sensory neurons. [score:4]
In our studies, we focused on miR-431, which was the most upregulated miRNA in DRG microarray after nerve injury in our experiments. [score:4]
The experiments revealed that only six genes (Braf, Eif2s2, Kremen1, Msi2, Tnrc6b, Zkscan1) were significantly down-regulated by miR-431 in PC12 cells (Table 1). [score:4]
The graph indicates a significant increase of miR-744, miR-431, and miR-21 in DRG after sciatic nerve crush, whereas the expression level of miR-124 and miR 29a did not change (* p < 0.05, ** p < 0.01, N = 3). [score:3]
To further reveal physiological role miR-431 Kremen1 interaction, we analyzed expression of Kremen1 at RNA and protein levels from control and regenerating DRGs. [score:3]
The function of Wnt signaling could potentially link our observation on increased miR-431 and decreased Kremen1 expression to the enhanced axonal outgrowth. [score:3]
Co-transfection with miR-431 mimics significantly reduced the luciferase activity (* p < 0.05, ** p < 0.01), whereas co-transfection with mimic negative controls did not affect the expression of firefly luciferase gene. [score:3]
miR-431 gain-of-function correlated with longer axons, more branches, and higher GAP-43 expression, a marker of regeneration. [score:3]
We observed a positive association between miR-431 expression and neurite outgrowth in dissociated DRG neuronal cell culture (Figure 2A). [score:3]
Overexpression of miR-431 significantly increased axon length. [score:3]
In contrast, transfection of miR-431 inhibitors impaired the regenerative axon growth, as significantly shorter axons and fewer branches were observed in DRG cultures. [score:3]
This relates to immunofluorescent data demonstrating significant increase in axon outgrowth after overexpression of miR-431. [score:3]
Transient overexpression of miR-431 was achieved using transfection of PC12 cells with miR-431 mimic. [score:3]
Applying miR-431 mimic to DRG neurons increased the expression level of miR-431 ß7.75-fold in DRG neuronal cell cultures (Figure 3A). [score:3]
Right panel depicts the effect of transection with miR-431 inhibitor. [score:3]
These results demonstrated that miR-431 level is inversely correlated to Kremen1 expression at mRNA level in DRG neurons. [score:3]
Kremen1 EXPRESSION IN DRG IN VIVOAfter establishing a physical interaction between miR-431 and Kremen1, we next investigated the expression patterns of Kremen1 during axon regeneration. [score:3]
miR-431, miR-714, miR-744, miR-877, miR-130b, miR-21, miR-323-3p, miR-325, miR-409-3p, miR-154*, and miR-681 were significantly increased 4 days post-sciatic nerve crush in pre-conditioned DRGs, while miR-190, miR-1, miR-33, miR-32, miR-153, miR-335-5p, miR-193, and miR-488 showed significantly decreased expression. [score:3]
Whole mount in situ hybridization revealed miR-431 localization to the developing spinal cord and brain with particularly strong expression in the pons. [score:3]
This effect on axon outgrowth is similar to the effect of miR-431 overexpression on axon outgrowth reported earlier (Figure 2B). [score:3]
Application of miR-431 inhibitors significantly elevated the mRNA level of Kremen1 (Figure 3C). [score:3]
We have further identified Kremen1 as the target that mediates the effects of miR-431 on neuronal cells. [score:3]
In the Ago-2 immunoprecipitated RNA samples, overexpression of miR-431 clearly increased the level of Ago-2 associated Kremen1 mRNA. [score:3]
We then applied the same approach to test these six genes with overexpression of miR-431 in primary DRG neurons. [score:3]
Together, these data suggest that miR-431 actively modulates Kremen1 protein and RNA expression within DRG neurons through association with Kremen1 3′UTR. [score:3]
miR-431 expression inversely relates to Kremen1. [score:3]
miR-431 MODULATES Kremen1 EXPRESSION AT mRNA AND PROTEIN LEVELS IN PRIMARY NEURONAL CULTURES. [score:3]
IDENTIFICATION OF miR-431 mRNA TARGETS. [score:3]
This may mean that miR-431 cleaves the mRNA of this gene rather than repressing its translation. [score:3]
Electrophoresis of CLIP samples confirmed the miR-431 induced association of Kremen1 mRNA with RISC, suggesting Kremen1 as the target gene for miR-431 (Figure 3B). [score:3]
The potential targets of miR-431 were chosen using three algorithms,, and. [score:3]
Negative controls for miR-431 mimic and inhibitor are indicated on the lower images. [score:3]
Effects of miR-431 mimic and inhibitor on axon outgrowth. [score:3]
Inhibition of cell viability by human IFN-beta is mediated by microRNA-431. [score:3]
LUCIFERASES REPORTER ASSAY CONFIRMS miR-431 TARGET Kremen1 3′UTR. [score:2]
In the total RNA samples from DRG cultures, overexpression of miR-431 reduced the amount of stable Kremen1 mRNA when compared to the miRNA mimic negative control group. [score:2]
Given the effects of miR-431 on Kremen1 expression and the role of miR-431 in neurite outgrowth, we investigated the effect of Kremen1 knockdown on regenerative axon growth. [score:2]
FUNCTIONAL ANALYSIS OF Kremen1 ROLE IN AXON REGENERATIONGiven the effects of miR-431 on Kremen1 expression and the role of miR-431 in neurite outgrowth, we investigated the effect of Kremen1 knockdown on regenerative axon growth. [score:2]
LUCIFERASES REPORTER ASSAY CONFIRMS miR-431 TARGET Kremen1 3′UTR Kremen1 has one binding site for miR-431 at its 3′-UTR, at the position 2530–2536 bp. [score:2]
To investigate a direct interaction between target mRNAs and miR-431 in RISC, CLIP of the Ago-2 protein, the central component of the RISC was carried out. [score:2]
Here we show that injury -induced miR-431 stimulates regenerative axon growth by silencing Kremen1, a negative regulator of Wnt/beta-catenin signaling pathway. [score:2]
To confirm miR-431 direct interaction on Kremen1 3′ UTR, we established a Kremen1 3′UTR-FLs construct with the 3′-UTR of Kremen1 inserted downstream of the FL gene. [score:2]
Using cross-linking with AGO-2 immunoprecipitation (CLIP), and 3′-UTR luciferase assay we demonstrate miR-431 direct interaction on the 3′-UTR of Kremen1 mRNA. [score:1]
After establishing a physical interaction between miR-431 and Kremen1, we next investigated the expression patterns of Kremen1 during axon regeneration. [score:1]
As shown in Figure 3F, co-transfection of miR-431 mimic and Kremen1 3′UTR-FL construct resulted in significant decrease in FL activity. [score:1]
We observed significant increase in GAP-43 immunostaining caused by transfection with miR-431 (Figure 2D). [score:1]
GAIN-OF-FUNCTION OF miR-431 INCREASES REGENERATIVE OUTGROWTH. [score:1]
Kremen1 has one binding site for miR-431 at its 3′-UTR, at the position 2530–2536 bp. [score:1]
However, to date, limited information is available about miR-431 physiological function. [score:1]
PC12 cells (40,000) were cultured and co -transfected in 24-well plates with 400 ng of FL reporter construct, 100 nM miR-431 mimics or mimic negative controls, and 40 ng of pRL-TK control vector encoding renilla luciferase (RL; Promega). [score:1]
miR-21: 5′-TAGCTTATCAGACTGATGTTGA-3′ miR-431: 5′-CAGGCCGTCATGCAAA-3′ miR-744: 5′-GGGCTAGGGCTAACAGCA-3′ miR-124: 5′-GCGGTGAATGCCAAAAA-3′ miR-29a: 5′-TAGCACCATCTGAAATCGGTTA-3′ Kremen1: 5′-ACAGCCAACGGTGCAGATTAC-3′ and 5′-TGT TGTACGGATGCTGGAAAG-3′ GAP-43: 5′TGGTGTCAAGCCGGAAGATAA-3′ and 5′-GCTG GTGCATCACCCTTCT-3′ S-12: 5′-TGGCCCGGCCTTCTTTATG-3′ and 5′-CCTAAGCG GTGCATCTGGTT-3′ Data from multiple independent experiments were analyzed with GraphPad Prism version 5 for Windows (GraphPad Software, San Diego, CA, USA). [score:1]
Both the gain-of-function of miR-431 and loss-of-function of Kremen1 significantly enhance regenerative axon growth in dissociated dorsal root ganglia (DRG) neuronal cultures. [score:1]
Increased mir-431 level was achieved by applying miR-431 mimic to DRG neuronal cell cultures at a final concentration of 100 nM. [score:1]
The effect of miR-431 on axon length (B) and on axon branching (C) was quantified. [score:1]
miR-21: 5′-TAGCTTATCAGACTGATGTTGA-3′ miR-431: 5′-CAGGCCGTCATGCAAA-3′ miR-744: 5′-GGGCTAGGGCTAACAGCA-3′ miR-124: 5′-GCGGTGAATGCCAAAAA-3′ miR-29a: 5′-TAGCACCATCTGAAATCGGTTA-3′ Kremen1: 5′-ACAGCCAACGGTGCAGATTAC-3′ and 5′-TGT TGTACGGATGCTGGAAAG-3′ GAP-43: 5′TGGTGTCAAGCCGGAAGATAA-3′ and 5′-GCTG GTGCATCACCCTTCT-3′ S-12: 5′-TGGCCCGGCCTTCTTTATG-3′ and 5′-CCTAAGCG GTGCATCTGGTT-3′ Data from multiple independent experiments were analyzed with GraphPad Prism version 5 for Windows (GraphPad Software, San Diego, CA, USA). [score:1]
PC12 cells were transiently transfected with miR-431 mimics or mimic negative controls, Kremen1 3′UTR-FL construct, and RL plasmid DNA as internal control. [score:1]
Taken together, Strickland’s and our study, demonstrate that miR-21 and miR-431 are implicated in peripheral nerve regeneration across species. [score:1]
miR-431 was initially identified as central nervous system specific miRNA as it was cloned from brain tissue of mouse embryos (Wheeler et al., 2006). [score:1]
Application of miR-431 mimics markedly increased the intracellular miR-431 level and promoted regenerative axon outgrowth. [score:1]
We validated the microarray data for miR-431 using real-time qPCR. [score:1]
DRG neuronal cell cultures were transfected with 100 nM of miR-431 mimic or a scrambled miRNA mimic negative control. [score:1]
Taken together, these results indicate that miR-431 mediates increase of axon growth through Kremen1 repression. [score:1]
THE FUNCTION OF miR-431 IN REGENERATIVE AXON GROWTH. [score:1]
Further studies are necessary to fully define the role of miR-431 in axonal regeneration. [score:1]
However, at this time, the function of miR-431 in the nervous system remains uncertain. [score:1]
The direct interaction between miR-431 and Kremen1 mRNA was confirmed by CLIP, and 3′-UTR luciferase reporter assay. [score:1]
In our study, Kremen1 loss-of-function produced an increase in axon outgrowth mimicking the effect of miR-431 gain-of-function but did not increase branching. [score:1]
We used three databases [1] to generate a list of mRNAs with potential binding site for miR-431 in their 3′-UTR. [score:1]
We observed that transient transfection with miR-431 mimic, decreased the mRNA level of Kremen1 to 30%. [score:1]
FIGURE 2 miR-431 increases axon outgrowth in DRG neurons. [score:1]
These data further support a functional relationship between miR-431 and Kremen1 in regenerating DRG neurons and suggest a role of Kremen1 in peripheral nerve regeneration. [score:1]
miR-21: 5′-TAGCTTATCAGACTGATGTTGA-3′ miR-431: 5′-CAGGCCGTCATGCAAA-3′ miR-744: 5′-GGGCTAGGGCTAACAGCA-3′ miR-124: 5′-GCGGTGAATGCCAAAAA-3′ miR-29a: 5′-TAGCACCATCTGAAATCGGTTA-3′ Kremen1: 5′-ACAGCCAACGGTGCAGATTAC-3′ and 5′-TGT TGTACGGATGCTGGAAAG-3′ GAP-43: 5′TGGTGTCAAGCCGGAAGATAA-3′ and 5′-GCTG GTGCATCACCCTTCT-3′ S-12: 5′-TGGCCCGGCCTTCTTTATG-3′ and 5′-CCTAAGCG GTGCATCTGGTT-3′Data from multiple independent experiments were analyzed with GraphPad Prism version 5 for Windows (GraphPad Software, San Diego, CA, USA). [score:1]
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2
[+] score: 66
These data indicate that miR-431 causes translational repression of Krm1 rather than mRNA degradation, which we observed in DRG culture in our previous publication (Wu and Murashov, 2013). [score:3]
Following incubation, the cells were transfected with either 100 nM hsa-miR-431-5p mimic or inhibitor using Lipofectamine 2000 (Thermo Fisher Scientific) reagent according to the manufacturer's protocol. [score:3]
We also asked how AβDDL treatment and transfection of the neuronal culture with miR-431 affects expression of Wnt signaling proteins including Dkk1, Krm1, β-catenin, and LRP6 at mRNA level. [score:3]
Effect of AβDDL and miR-431 treatments on expression of Wnt signaling proteins in cortico-hippocampal neurons. [score:3]
At the immunocytochemistry level, we also observed that treatment with miR-431 significantly reduced expression of Krm1 (Figures 6G–M). [score:3]
The experiment included the same treatment groups: control (vehicle treatment), AβDDL, miR-431, AβDDL+miR-431, AβDDL+miR-431+anti-miR inhibitor, AβDDL+miR-431+anti-miR negative control. [score:3]
Interestingly, we observed that miR-431 treatment of cortico-hippocampal culture significantly reduced expression of Krm1 at the protein level but not mRNA level. [score:3]
MicroRNA-431 regulates axon regeneration in mature sensory neurons by targeting the Wnt antagonist Krm1. [score:3]
These data indicate that miR-431 induced translational repression of Krm1 rather than mRNA degradation, which we observed in DRG culture in our previous publication (Wu and Murashov, 2013). [score:3]
In addition to rescuing synaptic sites, miR-431 treatment also reversed the inhibitory effect of AβDDL and Dkk1 on neurite outgrowth in 3-month WT, 6-month old WT, and 6-month 3xTg-AD animals, which was evident by the preserved neurite length and number of branches. [score:3]
Twenty-Four hours after treatment, neuronal cultures were fixed, and non-direct immunofluorescence against synaptic proteins was used to examine pre- and post-synaptic punctas from 3xTg-AD mice transfected with miR-431 prior to treatment with Dkk1 showed a significantly higher number of presynaptic sites (70.14 ± 3.097, n = 41) in comparison to cultures treated with Dkk1 and transfected with a negative mimic control (52.32 ± 3.343, n = 37, p < 0.005) (Figure 3A). [score:2]
Cortico-hippocampal cultures derived from 3 month old mice were transfected with either miR-431 or a negative mimic control. [score:1]
The number of presynaptic puncta sites in cultures treated with Dkk1 and transfected with miR-431 was 101.7 ± 3.535 (n = 15), while the number of presynaptic puncta sites in cultures treated with Dkk1 but not transfected with miR-431 was 80.06 ± 6.151 (n = 38) (Figure 4A). [score:1]
A number of post-synaptic sites in cultures treated with the negative mimic control and Dkk1 (54.47 ± 7.505) or AβDDL (59.65 ± 5.139, n = 19) were significantly lower in comparison to cultures transfected with miR-431 (Dkk1+miR-431: 107.6 ± 14.43, n = 8, p < 0.005; AβDDL+miR-431: M = 125.3 ± 11.87, n = 5, p < 0.001) (Figure 1B). [score:1]
Cortico-hippocampal cultures derived from 6-month old 3xTg-AD and WT mice were transfected with either miR-431 or a negative mimic control. [score:1]
Analyses of miR-431, Dkk1, Krm1, and Wnt in the brain were performed according to routine lab protocols (Wu et al., 2012). [score:1]
However, there was significant change in the amount of branching after Dkk1+miRNA-431 and AβDDL (Figure 2C). [score:1]
These results suggest that miR-431 treatment may delay AβDDL -associated synapse degeneration in the 3xTg-AD mouse mo del. [score:1]
The synaptic puncta is reduced after Aβ treatment (B) and preserved following miR-431 transection (C). [score:1]
Treatment with miR-431 prevented neurite degeneration following DKK1 and AβDDL treatments (Dkk1: 69.66 ± 3.474, n = 57; Dkk1+miR-431: 97.41 ± 3.648, n = 50 p < 0.0001; AβDDL: 63.97 ± 5.638, n = 14; AβDDL+miR-431: 97.81 ± 5.341, n = 14, p < 0.005) (Figures 3D, 6D–F). [score:1]
The number of post-synaptic sites in cultures treated with the negative mimic control and Dkk1 (71.32 ± 3.734, n = 16) or AβDDL (95.75 ± 6.883, n = 21) were significantly lower in comparison to cultures that also received treatment with miR-431 (Dkk1+miR-431: 139.8 ± 6.263, n = 9, p < 0.0001; AβDDL+miR-431: 141.2 ± 11.99, n = 12, p < 0.001) (Figure 2B). [score:1]
Figure 5 qRT-PCR analysis of Wnt signaling proteins after AβDDL and miR-431 treatments of cortico-hippocampal cultures of WT mice. [score:1]
Similar differences in synaptic puncta were observed between cultures treated with AβDDL and a negative microRNA mimic control (44.54 ± 3.747, n = 22) and cultures treated with AβDDL and miR-431 (92.43 ± 6.290, n = 16, p < 0.0001) (Figure 3A). [score:1]
In cortico-hippocampal cultures derived from 3xTg-AD and WT mice, application of miR-431 prevented Aβ -induced synapse degeneration and promoted neurite outgrowth. [score:1]
Effect of miR-431 treatment on synaptic puncta and neurite length after exposure to AβDDL and Dkk1 in 6-month old 3xTg-AD and WT mice. [score:1]
s derived from 6-month old 3xTg-AD and WT mice were transfected with either miR-431 or a negative mimic control. [score:1]
Neurite length in WT cultures was a more sensitive marker of the treatments with Dkk1, AβDDL and miR-431 (Figure 2D). [score:1]
The neurites degenerate after Aβ treatment (E) and protected following miR-431 transection (F). [score:1]
We have previously shown that Kremen1 (Krm1), a transmembrane receptor for Dkk1 and an antagonist of Wnt signaling, is specifically targeted by miR-431, which was confirmed by a pull-down-assay, an RT-qPCR, and a luciferase assay (Wu and Murashov, 2013). [score:1]
Cultures transfected with miR-431 followed by treatment with Dkk1 showed a significantly higher number of presynaptic sites (100.6 ± 4.851, n = 10) in comparison to cultures treated with Dkk1 and negative mimic control (45.96 ± 3.522, n = 18, p < 0.001) (Figure 2A). [score:1]
s derived from 3 month old mice were transfected with either miR-431 or a negative mimic control. [score:1]
Interestingly, treatment with AβDDL+miR-431+anti-miR induced an even bigger 2.7–3 fold increase in Dkk1 and Krm1 levels. [score:1]
s were transfected with miR-431 or a negative mimic control 48 h prior to treatment with AβDDL. [score:1]
The number of post-synaptic puncta in cultures treated with the negative mimic control and Dkk1 (51.13 ± 3.477, n = 36) or AβDDL (39.93 ± 3.471, n = 22) were significantly lower in comparison to cultures transfected with miR-431 (Dkk1+miR-431: 75.92 ± 4.802, n = 25 p < 0.001; AβDDL+miR-431: 82.36 ± 6.969, n = 15, p < 0.0001) (Figure 3B). [score:1]
Similar results were observed between cultures treated with AβDDL and negative mimic control (73.94 ± 2.631, n = 22) and cultures treated with AβDDL and miR-431 (94.06 ± 6.970, n = 17, p < 0.05) (Figure 2A). [score:1]
Significantly higher neurite length was observed in groups which received transfection with miR-431 and treatment with Dkk1 or AβDDL (Dkk1: 89.95 ± 4.522, n = 28; Dkk1+miR-431: 115.4 ± 7.309, n = 13, p < 0.05; AβDDL: 60.65 ± 4.620, n = 16; AβDDL+miR-431: 100.4 ± 5.931, n = 10, p < 0.001) (Figure 4D) vs. [score:1]
Cultures of 3-month WT mice transfected with miR-431 demonstrated significant recovery of (A) pre-synaptic puncta and (B) post-synaptic puncta in comparison to cultures treated with Dkk1. [score:1]
We observed that treatment with miR-431 prevented neurite degeneration following Dkk1 and AβDDL treatments (Dkk1: 68.50 ± 3.816, n = 12; Dkk1+miRNA-431: 105.8 ± 10.02, n = 8, p < 0.005; AβDDL: 60.65 ± 4.620, n = 16; AβDDL+miRNA-431: 100.4 ± 5.931, n = 10, p < 0.001). [score:1]
We have previously shown that peripheral nerve injury -induced miR-431 stimulates regenerative neurite growth in DRG sensory neurons by silencing Krm1, an antagonist of Wnt/beta-catenin signaling. [score:1]
Similarly, the number of presynaptic sites in cultures treated with AβDDL but not transfected with miR-431 was 72.33 ± 2.983 (n = 23) vs. [score:1]
Specifically, we observed a rescue of pre- and post-synaptic puncta after transfection with miR-431 in AβDDL and Dkk1 treated cultures. [score:1]
Cultures from 3xTg-AD mice transfected with miR-431 followed by treatment with Dkk1 showed a significantly higher number of presynaptic sites (116.7 ± 12.12, n = 9) in comparison to cultures treated with Dkk1 and negative mimic control (52.17 ± 7.788, n = 7, p < 0.0001) (Figure 1A). [score:1]
The number of post-synaptic puncta in cultures treated with Dkk1 (102.1 ± 8.381, n = 27) and AβDDL (85.44 ± 4.792, n = 19) were not significantly different from number of puncta in cultures that were transfected with miR-431 (Dkk1+miR-431: 136.5 ± 5.162, n = 11; AβDDL+miR-431: 116.1 ± 6.637, n = 9) (Figure 4B). [score:1]
Cultures of 3-month 3xTg mice transfected with miR-431 demonstrated significant increase in (A) pre-synaptic puncta and (B) post-synaptic puncta in comparison tp cultures treated with Dkk1, relative to control. [score:1]
s of 6-month 3xTg mice transfected with miR-431 demonstrated significantly higher number of (A) pre-synaptic puncta and (B) post-synaptic puncta in comparison to cultures treated with Dkk1. [score:1]
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3
[+] score: 22
In contrast to the up-regulated miRNAs in pluripotent state, down-regulated miRNAs directly target the core pluripotency factors like miRNA431 targeting Sox2 (Additional file 1: Figure S5). [score:12]
Surprisingly, we only found one miRNA (miR-684) that barely up-regulated (~2 fold changed) [18, 24] (GEO database, methods and materials) in the pluripotent state and directly binds to Sox2 (Fig.   4e), which was also targeted by down-regulated miRNA-431. [score:10]
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[+] score: 12
Among the 7 miRNAs dynamically regulated over the course of normal lung development (Group A), 5 of these miRNAs (miR-411, miR-431, miR-699, miR-29a and miR-29c) were up-regulated by oxygen exposure, suggesting that prolonged hyperoxia alters the expression of miRNAs utilized during normal lung development. [score:9]
In Group A, the expression values of four miRNA were decreased (Pattern 1; miR-322*, miR-411, miR-431, miR-609) and three were increased (Pattern 2; miR-146b, miR-29a, miR-29c). [score:3]
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5
[+] score: 9
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Out of these 25 miRNAs, 18 miRNAs were differentially expressed in a consistent manner between the 2 groups (Figure 4A, highlighted); 8 miRNAs were downregulated in both groups (miR-16, miR-200, miR-205, miR-3064, miR-379, miR-431, miR-485 and miR-491) and 10 miRNAs were upregulated in both groups (miR-194, miR-1894, miR-211, miR-3072, miR- 3077, miR-4436, miR-5128, miR-669a, miR-669c and miR-6967). [score:9]
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[+] score: 9
The second gene of interest is Nmnat1, which was downregulated (–1.24-fold change and P=0.01), whereas its three predicted target miRNAs (mir-1224, mir-431 and mir-743a) were upregulated (Fig. 7). [score:9]
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The TaqMan® Array Human MicroRNA Card contained all 13 possible miRs predicted to target IRAK-1, and 24 h HG-stimulation caused the downregulation of seven endothelial miRs: miR-146a-5p, miR-339-5p, miR-874-3p, miR-125-3p, miR-431-5p, miR-192-5p, and miR-215-5p (Figure 2A). [score:6]
HG stimulation for 24 h revealed that seven miRs, miR-146a-5p, miR-339-5p, miR-874-3p, miR-125-3p, miR-431-5p, miR-192-5p, and miR-215-5p, were downregulated by HG, as compared with unstimulated control. [score:3]
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[+] score: 6
miR-2136, let-7f-5p, miR-431-5p, and miR-491-3p were upregulated in both 3-month-old and 6-month-old AD mice, implying their role in the development of AD. [score:5]
Furthermore, levels of miR-2136, let-7f-5p, miR-431-5p, and miR-491-3p were higher in both 3-month-old and 6-month-old APP/PS1 mouse brain, indicating their potential involvement in the progression of AD (Figure 2). [score:1]
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We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
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[+] score: 4
Three microRNAs in this region, miR-431, miR-127, and miR-136, were shown previously to regulate Peg11 through a siRNA-like mechanism [52]. [score:2]
org/microrna/) Meg3mmu-miR-770 # Bmp1, Bmp15, Capn3, Casq2, Fosb, Lmna, Mb, Obscn, Peg10, Ppp1ca, Sspn, Tmod1, Trp53 Unidentified mmu-miR-673 Camk2a, Camk2b, Camk2d, Camk2g, Dnmt1, Mtpn, Myh6, Ndn, Pax3, Rbl1, Sln, Tnnt1, Wnt1 Unidentifiedmmu-miR-493 # Cacng5, Camk2g, Cdkn1c, Ctcf, Dag1, Fhl1, Fos, Hras1, Jun, Mib2, Mtap, Peg10, Shh, Tmod1 Unidentifiedmmu-miR-337 # Capza2, Des, Dmd, Dnmt3a, Myh8, Mypn, Nfatc1, Plagl2, Pvalb, Sgcb, Snta1, Tpm3, Trp53 Unidentified mmu-miR-540 Akt3, Bmp2, Bmp7, Capzb, Emd, Itga7, Itgb1, Msc, Myog, Nkx2-5, Pten, Rhoa, Sln, Tlx1, Vim Unidentifiedmmu-miR-665 # Casq2, Igf2, Junb, Ldb3, Peg10, Magel2, Nnat, Pax3, Ryr1, Sntb2, Tln1, Tpm2, Trp53, TtnAnti-Peg11 $ mmu-miR-431 # d Camk2b, Casq1, Dtna, E2f1, Fgf4, Gata3, Igf1, Kit, Max, Peg10, Plagl2, Ppp3r1, Sgcd, Tcf21Anti-Peg11 $ mmu-miR-433 # Bmpr1b, Capza1, Creb1, Ctcf, E2f3, Gata6, Isl1, Jak2, Myh9, Peg10, Plagl2, Ppp3r1, Sntg1Anti-Peg11 $ mmu-miR-127 # d e Auts2, Bcl6, Camk2d, Cdc42, Creb5, E2f3, Igf2, Myo1c, Otx1, Plagl2, Pitx2. [score:1]
This conclusion is based on the observation that our cDNA begins at the end of miR-431 precursor and ends at the beginning of miR-127 precursor. [score:1]
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Among these, a short cluster of maternally expressed miRNAs genes (miR-431, miR-433, miR-127, miR-434 and miR-136) is transcribed and processed from an antisense gene to the paternally expressed Retrotransposon-like 1 (Rtl1) gene, the recently characterized protein product of which appears to be indispensable for mouse foetal development [37]. [score:4]
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It is possible that such an overlapping gene structure may also exist for other miRNAs, such as miR-431 and miR-433. [score:1]
It is possible that the genes encoding miR-431 and miR-433 may also overlap and that this small transcript may represent pri-miR-431. [score:1]
We are undertaking the effort to identify the transcriptional initiation and termination sites for pri-miR-431 and determine if pri-miR-431 overlaps with pri-miR-433. [score:1]
MiR-431 is located about 1 kb upstream from miR-433. [score:1]
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Our results are consistent with a recent study by Wu et al., wherein the expression of miR-431 derived from the Dlk1-Dio3 locus is increased in myostatin knockout mice [23]. [score:4]
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In the Dlk1-Dio3 region, the maternally expressed genes can produce non-coding RNAs, including mir-431, mir-433, mir-127, mir-432 and mir-136. [score:3]
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A recent study that provided male mice with 12 weeks of voluntary wheel-running reported changes in the expression levels of miR-483, miR-431, miR-21 and miR-221 in sperm. [score:3]
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The rest of the differentially expressed miRNAs between strains have been found to be altered in different neurodegenerative mo dels (28a-5p, miR-337-3p, miR-431-5p, miR-455-5p). [score:3]
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In addition, accumulating evidence suggests that the aberrant expressions of miRNAs, such as miR-1, miR-133, miR-23a, miR-206, miR-27, miR-628, miR-431 and miR-21 (refs 17, 18, 19, 20, 21, 22, 23, 24), contribute to muscle atrophy. [score:3]
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The physiology and pathology of skeletal muscle are profoundly influenced by microRNAs such as miR-1, miR-133, miR-206, miR-29, and miR-431 [19– 21]. [score:1]
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Several of these miRNAs (mir-299, mir-431, mir-467c, mir-222, mir-32, mir-330, mir-384, mir-665, and mir-671) have previously been identified as sex-biased in the neonatal mouse whole brain and/or rat cortex [23, 48]. [score:1]
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Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
Other families that had a high abundance of reads were miR-134, miR-136, miR-154, miR-370, miR-412, miR-431, miR-432, miR-433, miR-485, miR-493, miR-541; a total of 11 miRNA families. [score:1]
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As an example, miR-322 and miR-431, that were mapped on chromosome 1 (51–59 Mb), are clustered in the ‘red’ module. [score:1]
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